Open AccessBiotin rescues mitochondrial dysfunction and neurotoxicity in a tauopathy model
Author(s) -
Kelly M. Lohr,
Bess Frost,
Clemens R. Scherzer,
Mel Β. Feany
Publication year - 2020
Publication title -
proceedings of the national academy of sciences
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 5.011
H-Index - 771
eISSN - 1091-6490
pISSN - 0027-8424
DOI - 10.1073/pnas.1922392117
Subject(s) - tauopathy , neuroprotection , neurotoxicity , frontotemporal dementia , neuroscience , dementia , neurodegeneration , biology , disease , druggability , tau protein , medicine , bioinformatics , genetics , alzheimer's disease , pathology , gene , toxicity
Significance Pathological tau accumulation is implicated in a variety of neurodegenerative diseases, including frontotemporal dementia and Alzheimer’s disease. Based on a large-scale forward genetic screen inDrosophila , our study highlights a modifier of tau neurotoxicity, the enzyme biotinidase. Our results suggest that biotin status may represent a druggable metabolic pathway and a potential therapeutic approach to neuroprotection in human tauopathies.
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